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Reading, MA: Addison-Wesley. Original edition, Complex Systems 1, pp. 495-502. Technical report CMU-CS-86--128, Carnegie Mellon University. 1987.

Moss, Lenny. 2001. Deconstructing the gene and reconstructing molecular develomentalsystems. In Cycles of Contingency: Developmental Systems and Evolution, editedby S. Oyama, P. E. Griffiths and R. D. Gray. Cambridge, Mass.: MIT Press.

———. 2002. What Genes Can't Do. Cambridge, MA: MIT Press.Odling-Smee, F. John, Kevin N Laland, and Marcus W Feldman. 2003. Niche

Construction: The Neglected Process in Evolution. Vol. 37, Monographs inPopulation Biology. Princeton, NJ: Princeton University Press.

Papineau, David. 2003. The Baldwin Effect and Social Learning. Paper read at Innatenessand the Structure of the Mind, July 2003, at Sheffield.

———. 2005. Social Learning and the Baldwin Effect. In Cognition, Evolution, andRationality, edited by A. Zilhão. London: Routledge.

Preston, Katherine, and Massimo Pigliucci, eds. 2004. The Evolutionary Biology ofComplex Phenotypes. Oxford and New York: Oxford University Press.

Schlichting, Carl D. 2003. Environment. In Keywords and Concepts in EvolutionaryDevelopmental Biology, edited by B. K. Hall and W. M. Olson. Cambridge, MAand London: Harvard University Press.

Simpson, George Gaylord. 1953. The Baldwin Effect. Evolution 7 (June):110-117.Sterelny, Kim, and Paul E Griffiths. 1999. Sex and Death: An Introduction to the

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Waddington, Conrad H. 1942. Canalisation of development and the inheritance ofacquired characters. Nature 150:563-565.

———. 1952. The evolution of developmental systems. Paper read at Twenty-eighthMeeting of the Australian and New Zealand Association for the Advancement ofScience, at Brisbane, Australia.

———. 1953. The "Baldwin Effect", "Genetic Assimilation" and "Homeostasis".Evolution 7 (4):386-387.

———. 1953. Genetic assimilation of an acquired character. Evolution 7:118-26.Wagner, Günther P, ed. 2001. The Character Concept in Evolutionary Biology. : . San

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canalization. Evolution 51 (2):329-347.Weber, Bruce H., and David J. Depew, eds. 2003. Evolution and Learning: The Baldwin

effect Reconsidered. Cambridge, Mass.: MIT Press.Wilkin, Adam. 2003. Canalization and Genetic Assimilation. In Keywords and Concepts

in Evolutionary Developmental Biology, edited by B. K. Hall and W. M. Olson.Cambridge, MA and London: Harvard University Press.

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Ariew, André. 1996. Innateness and Canalization. Philosophy of Science 63 (3(Supplement)):S19-S27.

———. 1999. Innateness is Canalization: In Defense of a Developmental Account ofInnateness. In Where Biology Meets Psychology: Philosophical Essays, edited byV. G. Hardcastle. Cambridge, Mass.: MIT Press.

Bateson, Patrick P G. 2004. The Active Role of Behaviour in Evolution. Biology &Philosophy 19 (2):283-298.

Belew, R.K, and M Mitchell, eds. 1996. Adaptive Individuals in Evolving Populations.Reading, Mass.: Addison-Wesley.

Brakefield, Paul M, and Pieter J Wijngaarden. 2003. Phenotypic Plasticity. In Keywordsand Concepts in Evolutionary Developmental Biology, edited by B. K. Hall andW. M. Olson. Cambridge, MA and London: Harvard University Press.

Falk, Raphael. 2000. The Gene: A concept in tension. In The Concept of the Gene inDevelopment and Evolution, edited by P. Beurton, R. Falk and H.-J. Rheinberger.Cambridge: Cambridge University Press.

Gass, Gillian L, and Jessica M Bolker. 2003. Modularity. In Keywords and Concepts inEvolutionary Developmental Biology, edited by B. K. Hall and W. M. Olson.Cambridge, MA and London: Harvard University Press.

Gilbert, Scott F, John M Opitz, and Rudy A Raff. 1996. Resynthesising evolutionary anddevelopmental biology. Developmental Biology 173:357-372.

Gilbert, Scott F. 2001. Ecological Developmental Biology: Developmental Biology meetsthe Real World. Developmental Biology 233:1-22.

Griffiths, Paul E. 2003. Beyond the Baldwin Effect: James Mark Baldwin's 'socialheredity', epigenetic inheritance and niche-construction. In Evolution andLearning: The Baldwin Effect Reconsidered, edited by B. H. Weber and D. J.Depew. Cambridge, Mass.: MIT Press.

———. 2004. Instinct in the '50s: The British Reception of Konrad Lorenz's Theory ofInstinctive Behaviour. Biology and Philosophy 19:xxx-xxx.

Griffiths, Paul E, and Eva M Neumann-Held. 1999. The many faces of the gene.BioScience 49 (8):656-662.

Haldane, J. B. S. 1992 [1955]. Animal Communication and the Origin of HumanLanguage. Current Science 63 (9-10):604-611.

Haldane, J. B. S., and Helen Spurway. 1954. A statistical analysis of communication in"Apis Mellifera" and a comparison with communication in other animals. InsectesSociaux 1 (3):247-284.

Hall, Brian K. 1992. Waddington's legacy in development and evolution. AmericanZoologist 32:201-205.

———. 1999. Evolutionary Developmental Biology. 2 ed. Dordrecht: Kluwer.———. 2003. Baldwin and Beyond: Organic Selection and Genetic Assimilation. In

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Hinton, G.E, and S.J Nowlan. 1996. How Learning can Guide Evolution. In AdaptiveIndividuals in Evolving Populations, edited by R. K. Bewel and M. Mitchell.

21

examine the selection pressures on the specific loci involved in making the switch

between the dependence of a behavior on learning and its independence of learning, as

Papineau does. But this should not be confused with the quite different project in which

Waddington was engaged, namely asking how developmental systems make such options

readily available to selection.

5. Conclusion

Many evolutionary processes have been described in which a trait that initially develops

in the members of a population as a result of some interaction with the environment

comes to develop without that interaction in their descendants. Waddington’s genetic

assimilation is importantly different from the rest of this ‘Baldwiniana’ because his

explanatory focus was not on the selection pressures at the point of transition, but on how

developmental systems come to be structured in such a way that these evolutionary

transitions are readily accessible to evolving lineages. Waddington’s approach also

replaces the simple contrast between ‘acquired’ and ‘innate’ with a non-dichotomous

model of developmental canalisation and phenotypic plasticity that is in line with recent

work on the evolution of development. From a Waddingtonian perspective evolutionary

transitions between ‘innate’ and ‘acquired’ are only to be expected because those

categories have little meaning in terms of developmental genetics and in some cases the

difference between the ‘innate’ and ‘acquired’ may require only a minimal change in

developmental mechanisms. But to see this it is necessary to use a gene concept suitable

for thinking about development, and not a gene concept designed for theoretical

population genetics or for the prediction of phenotypic differences within populations.

20

chromosome is a Gene-P with respect to the masculinisation of the foetus: individuals

who have this gene are very likely to have a male phenotype. But it does not follow that

the evolution of sexual differentiation should be studied by asking how the SRY gene

evolved. The masculinisation of the mammalian foetus is the result of a complex cascade

of a gene expression. Both male and female foetuses have almost all the genes involved

in this cascade. In Waddington’s terms the developmental landscape has a deep

branching valley running across it and the SRY gene, or its equivalent in other mammals,

simply nudges the foetus into one branch rather than the other. With this picture in mind,

it is easy to understand how two rodents of the genus Ellobius have managed to lose the

whole Y chromosome whilst retaining the gene expression cascade of mammalian sexual

development. Some other gene expression event early in development acts to triggers the

same cascade. Furthermore, sexual differentiation is an ancient characteristic of

vertebrates and in this larger group cascades of gene expression that are to some degree

homologous with those in mammals are triggered in still more diverse ways. Crocodiles,

amongst others, have environmentally triggered sexual differentiation. Some fish retain

the capacity for females to be masculinised by an environmental trigger throughout their

life cycle. From the viewpoint of developmental genetics, understanding the evolution of

the specific triggering cause in one group or another is not the way to understand the

evolution of the cascade of gene expression which constitutes becoming male.

Nevertheless, there is nothing wrong with Gene-P thinking in the right context – if we

want to ask about the evolutionary pressures leading to genetic versus environmental sex

determination it is appropriate to pose the question in terms of the selection pressures on

the specific loci involved in these two modes of triggering. In the same way, we could

19

scenarios designed to address these questions are Gene-Ps corresponding to the

difference between the first trait and the second.

In contrast, most of the genes that figure in Waddington’s genetic assimilation scenario –

the ‘pegs’ in Figure 1 – are genes that are present both when the trait is dependent on the

environment and when it is independent of the environment. They are the genes (Gene-

Ds) which play a causal role in building the K phenotype, not the genes that differ

between cases where that particular cascade of gene expression is switched on

endogenously and cases where it is switched on exogenously or even the genes that differ

between individuals that have K and those that lack K. The evolutionary problem is

framed as follows: How does evolution produce traits which can be readily switched

between different triggers? This second way of thinking about how the development of a

phenotypic trait can become independent of certain aspects of the developmental

environment corresponds to some of major themes in recent evolutionary developmental

biology, namely the evolution of developmental modularity (Gass and Bolker 2003;

Wagner 2001) and the evolution of phenotypic plasticity (Preston and Pigliucci 2004;

Gilbert 2001; Brakefield and Wijngaarden 2003). These evolutionary problems simply

cannot be posed if evolution is represented as change over time in the frequency of

‘genes for’ specific phenotypes (Gene-Ps).

We can compare these two ways of thinking about how the development of a phenotypic

trait can become independent of certain aspects of the environment with two ways to

approach the evolution of sexual differentiation. The primate SRY gene on the Y

18

‘environmental assimilation’ when the selection pressures are reversed. ‘Baldwinian’

phenomena are thus subsumed under the more general topic of the selective advantages

of different patterns of interaction between gene and environment – the field of research

known today as ‘adaptive phenotypic plasticity’ (Brakefield and Wijngaarden 2003;

Schlichting 2003). The traditional emphasis on the Baldwin effects and its relatives to the

exclusion of other evolutionary patterns reflects a misguided desire to get the effects of

the environment on development ‘written into the germline’, which in turn reflects the

mistaken conviction that only in this way can the effects of the environment on

development be of evolutionary significance (Griffiths 2003).

4. Gene concepts and explanatory foci

In the evolutionary scenario described by Papineau the gene for trait K (‘allele KG’)

spreads through the population in response to a selection pressure caused by the spread of

a learnt trait T whose acquisition requires of five separate dispositions to each of which

corresponds to a gene (‘allele KL’ and four companions). As I remarked above, these

genes are Gene-Ps - DNA elements individuated by the criteria that their presence is a

reliable statistical predictor of a phenotypic difference. This, I suggest, is typical of one

way of thinking about how the development of a phenotypic trait can become

independent of certain aspects of the developmental environment. The evolutionary

problem is framed as follows: 1) What are the adaptive advantages of having T

conditional on an environmental factor? 2) What are the adaptive advantages of having T

independent of that factor? 3) Does the evolution of the first trait produce new selection

pressures which favour the evolution of the second? The genes that feature in typical

17

I have discussed elsewhere how some of Waddington’s contemporaries, particularly

J.B.S Haldane and his wife and collaborator Helen Spurway, saw his work on genetic

assimilation as demonstrating that there need be little difference as regards

developmental genetics between ‘innate’ and ‘acquired’ traits (Griffiths 2004). Haldane

and Spurway drew on Waddington to argue that transitions back and forth between

instinct and learning were to be expected in response to the adaptive advantages of these

two forms of development in specific environments. A couple of brief quotations will

give the flavour of this work:

(discussing passerine song learning) “some of these species must have passed through

a stage where the song was learnt by some individuals and was instinctive in others.

As a geneticist I think that it is quite impossible to make a sharp distinction between

learnt and unlearnt behavior.” (Haldane 1992 [1955], 605).

“The number of generations during which a learned ethogenesis evolves into an

instinctive ethogenesis, if it does so at all, depends on the relative strength of the

selection pressures favouring uniformity and variability in development.”(Haldane and

Spurway 1954, 275)

One of the most exciting features of this, Waddingtonian, vision of transitions between

instinct and learning is its symmetry. Most accounts of the Baldwin effect and its

relatives focus exclusively on the elimination of dependence on an environmental factor,

but the mechanisms underlying Waddington’s genetic assimilation can equally lead to

16

We are now in a position to see why Waddington thought there would be little difference

between the actual developmental processes that underlie a highly canalised phenotype

that depends on an environmental stimulus and those that underlie one that has been

rendered independent of that stimulus. Waddington writes:

“If natural selection was in this way acting in favour of the ability to respond in a

useful way to some environmental stimulus, it would also in time build up a

canalised response, so that the most valuable degree of expression was regularly

achieved. Once that had been done, the genotype would have been modified so

that it determined a new valley on the developmental surface; but it would still

require the push of an environmental stimulus to cause one of the balls in our

model to run into it. However, once the valley was formed and canalised, the

exact strength of the push, and the exact time at which it was applied, would be of

lesser importance. In fact, we might expect that, by this stage in the evolution

[sic], there would be a number of mutant genes available in the species which

could divert development into the prepared channel; and thus, once the ground

had been prepared, as it were, an internal genetic mechanism could take over from

the original environmental stimulus. We can thus envisage a mechanism by which

a valuable response to the environment could become gradually incorporated into

the hereditary endowment of the species.” (Waddington 1952, 159)

15

we are not forced to draw this distinction. The idea of canalisation with respect to all the

parameters that are included in a model of the developmental system is equally

legitimate. It is, after all, far from clear whether to classify many critical parameters, such

as the presence of DNA methylation or of maternal gene products in the cytoplasm, as

‘genetic’ or ‘environmental’. The issue of genes versus environment is peripheral to

Waddington’s central concern, which is how developmental outcomes can be robust and

reliable in the face of variations in developmental parameters.

Like some modern authors, Waddington believed that natural selection would favor the

canalisation of important adaptive phenotypes. Developmental systems that produce

important adaptive outcomes robustly will be selected over those that are easily

perturbed. Although I do not have time to explore this theme fully here, it is important to

recall that, like his contemporaries I.I Schmalhausen and Theodosius Dobzhansky,

Waddington saw natural selection as optimizing, not the phenotypic character itself, but

rather a norm of reaction which specifies a range of phenotypes as a function of genetic

backgrounds and environmental conditions: “An animal is, in fact, a developmental

system, and it is these systems, not the mere static adult forms which we conventionally

take as typical of the species, which become modified in the course of evolution”

(Waddington 1952, 155). When there is a single, optimal phenotype, ‘stabilising

selection’ will operate to select a narrow reaction norm, or, in other words, to canalize the

phenotype. In other circumstances, however, selection may favour a broader reaction

norm, producing what we describe today as ‘adaptive phenotypic plasticity’. The shape of

the norm of reaction is itself a character produced by natural selection.

14

In a series of widely-read papers the philosopher Andre Ariew has used Waddington’s

concept of canalisation to explicate the concept of innateness (Ariew 1996, 1999). Innate

traits, Ariew has argued, are those traits insensitive to environmental variation, or,

equivalently, those traits which are canalised with respect to changes in the

environmental parameters of a developmental system. Unfortunately, Ariew’s work has

led philosophers who know of Waddington only through these papers to use the term

‘canalisation’ and even ‘genetic canalisation’ to mean insensitivity to environmental

variation. In fact, the idea of insensitivity to environmental factors, properly known as

‘environmental canalisation’ (Wagner, Booth, and Homayoun 1997), cannot even be

represented in Waddington classic picture of the developmental landscape (Figure 1).

Environmental parameters are not included in this model, and whether a phenotype is

canalised in Waddington’s original sense is a question of the dynamical structure of the

developmental system, not the relative role of genes and environment5. But the model can

easily be extended to include environmental parameters, and Waddington himself does so

when discussing genetic assimilation, as seen below. If these additional parameters are

added, then we can define both ‘environmental canalisation’ and ‘genetic canalisation’. A

phenotypic outcome is environmentally canalised if those features of the surface which

direct development to that endpoint are relatively insensitive to the manipulation of

environmental parameters. A phenotypic outcome is genetically canalised if those

features of the surface which direct development to that endpoint are relatively

insensitive to the manipulation of genetic parameters. It should be noted, however, that

5 The evolutionary developmental biologist Brian Hall has written extensively on Waddington and hasstressed that his thought was profoundly ‘gene centered’ in the sense that he saw the developmental systemas primarily and predominantly the expression of a potential present in the genome (Hall 2003, 1992,1999).

13

Thus, in Waddington’s vision, phenotypes are global expressions of genomes, but it does

not follow that particular parts of the phenotype express particular parts of that genome.

The gene concept that fits this thoroughly epigenetic view of development is the one

which Moss has labeled ‘Gene-D’:

“Quite unlike Gene-P, Gene-D is defined by its molecular sequence. A Gene-D is

a developmental resource (hence the “D”) which in itself is indeterminate with

respect to phenotype. … To be a gene for N-CAM, the so-called “neural cell

adhesion molecule,” for example, is to contain the specific nucleic acid sequences

from which any of a hundred potentially different isoforms of the N-CAM protein

may potentially be derived … N-CAM molecules are (despite the name)

expressed in many tissues , at different developmental stages, and in many

different forms. The phenotypes of which N-CAM molecules are co-constitutive

are thus highly variable, contingent upon the larger context, and not germane to

the status of N-CAM as a Gene-D.” (Moss 2001, 88, his emphases)4

To understand Waddington’s vision of development it is essential not to think of genes as

‘genes for’ particular phenotypes or phenotypic differences (Gene-P), but instead to think

of them as parameters of a developmental system (Gene-D). It is necessary to think in

terms of what in Waddington’s day was known as ‘physiological genetics’.

4 Philosophers will note that Gene-P and Gene-D correspond respectively to ‘descriptive’ and ‘rigid’readings of the phrase ‘the gene for T’ when this phrase is used in the usual way to report the fact that someDNA sequence accounts for a large portion of the variance in trait T in some study population (SeeSterelny and Griffiths 1999, 90-92).

12

In modern terms, Waddington’s ‘developmental landscape’ is a representation of

development as complex system whose parameters are genetic loci and whose state space

is a set of phenotypic states. The state space is depicted as a surface, each point of which

represents a phenotype. The genetic parameters are depicted as pegs that pull on the

surface and thus determine its contours. Epistatic interactions between loci are

represented by links between the cords by which those loci pull on the surface. The

development of an organism over time is represented by the movement of a ball over the

surface, which is dictated by gravity, so that the ball rolls downhill on a path dictated by

the contours of the surface. The development of the organism is thus represented by its

trajectory over the surface, through successive phenotypic states. The basic point which

Waddington uses this representation to make is that if the surface has any significant

contours, then the effect of a change at one genetic locus will be dictated by the overall

shape of the landscape, which is a global consequence of the states of all the other genetic

loci. Some genetic changes, such as those which affect the tops of inaccessible ‘hills,’

will have no effect on development. Other changes of the same intrinsic genomic

magnitude which affect the entrance of a valley or ‘canal’ will have a massive effect on

development. The phenotypic impact of a genetic change is not proportional to the

magnitude of the genomic change, but depends on the overall dynamics of development.

Furthermore, the phenotypic difference produced by a genetic difference is not explained

by that genetic difference in itself, but by how that change interacts with the rest of the

developmental system. This picture retains considerably validity in the light of

contemporary developmental genetics (Gilbert, Opitz, and Raff 1996; Wilkin 2003)

11

Figure 1. Waddington's ‘ developmental landscape’. (a) The developmental trajectory of

the organism, represented by the rolling ball, is determined by a landscape representing

the developmental dynamics of the organism. (b) The shape of this landscape is

determined by genes, here represented by pegs pulling the landscape into shape via

strings, and by epistatic interactions between genes, here represented by connections

between strings. From Waddington (1957: 36).3

3 Note to editor: Copyright request to: Allen & Unwin Ltd., 19 Crompton Terrace,London, N1 2UN, for pg.36 of 'The Strategy of the Genes - A Discussion of SomeAspects of Theoretical Biology'; C.H. Waddington; Ruskin House (copyright GeorgeAllen & Unwin Ltd.); 1957.

10

than by the influence of one or a few specific alleles. Thus, for example, Waddington

sought to explain one of the major biological discoveries of his day – the fact that

extreme phenotypic uniformity can be observed in many wild populations despite

extensive genetic variation in those same populations – by appealing to the global

dynamics of developmental systems. A ‘canalised’ developmental system takes

development to the same endpoint from many different genetic starting points. The

development of wild-type phenotypes can thus be buffered against genetic variation.

Waddington represented this idea with his famous ‘developmental landscape’ (Figure 1).

9

3. Genetic Assimilation and Gene-D

Waddington was aware that his vision of development required a conception of the gene

which does not intrinsically link genes and specific phenotypic outcome. He made this

point in ‘The Evolution of Developmental Systems’, an address delivered in Brisbane in

1951:

“Some centuries ago, biologists held what are called “preformationist” theories of

development. They believed that all the characters of the adult were present in the

newly fertilized egg, but packed into such a small space that they could not be

distinguished with the instruments then available. If we merely consider each

gene as a determinant for some definite character in the adult (as when we speak

loosely of the ‘gene for blue eyes, or for fair hair’), then the modern theory may

appear to be merely a new-fangled version of the old idea. But in the meantime,

the embryologists, who are concerned with the direct study of development, have

reached a quite different picture of it … This is the theory known as epigenesis,

which claims that the characters of the adult do not exist already in the newly

fertilized germ, but on the contrary arise gradually through a series of causal

interactions between the comparatively simple elements of which the egg is

initially composed. There can be no doubt nowadays that this epigenetic point of

view is correct.” (Waddington 1952, 155)

In Waddington’s vision of development, the entire collection of genes makes up a

developmental system which produces a phenotype. Many features of the phenotype are

explained by the dynamical properties of that developmental system as a whole, rather

8

KG individuals acquire T more reliably than KL individuals. The sought-for link between

individuals initially learning the sub-trait K and later individuals possessing K without

learning is mediated by a process of niche construction – a change in the selective regime

as a result of behavior. In contrast, Waddington thought that the link between the ability

to reliably acquire an adaptive trait and the appearance of individuals with an intrinsic

tendency to exhibit that trait was forged by the typical nature of the development

pathways underlying adaptively valuable traits. It was for this reason that he objected to

Simpson’s term ‘Baldwin effect’ with its implication that this evolutionary process is a

special case. Waddington intended genetic assimilation to be a ubiquitous feature of

phenotypic evolution:

“Simpson comes to the conclusion that the Baldwin effect, in the sense he describes it,

has probably played a rather small role in evolution. The genetic assimilation

mechanism, however, must be a factor in all natural selection, since the properties

with which that process is concerned are always phenotypic; properties, that is, which

are the products of genotypes interacting with environments.”(Waddington 1953, 386)

According to Waddington the tendency of phenotypes to become genetically assimilated

reflects the fact that there is little difference between the actual developmental processes

that underlie a highly canalised phenotype that depends on an environmental stimulus and

one that has been rendered independent of that stimulus, as I will now try to explain.

7

2. Genetic Assimilation and Gene-P

In the passage quoted above Papineau employs a concept of the gene which Lenny Moss

has labeled ‘Gene-P’:

“Gene-P is defined by its relationship to a phenotype. … Gene-P is the expression

of a kind of instrumental preformationism (thus the “P”). When one speaks of a

gene in the sense of Gene-P one simply speaks as if it causes the phenotype. A

gene for blue eyes is a Gene-P. What makes it count as a gene for blue eyes is not

any definite molecular sequence (after all, it is the absence of a sequence based

resource that matters here) nor any knowledge of the developmental pathway that

leads to blue eyes (to which the "gene for blue eyes" makes a negligible

contribution at most), but only the ability to track the transmission of this gene as

a predictor of blue eyes. Thus far Gene-P sounds purely classical, that is,

Mendelian as opposed to molecular. But a molecular entity can be treated as a

Gene-P as well. BRCA1, the gene for breast cancer, is a Gene-P, as is the gene for

cystic fibrosis, even though in both cases phenotypic probabilities based upon

pedigrees have become supplanted by probabilities based upon molecular

probes.” (Moss 2001, 87-88)

Papineau’s five genes are Gene-Ps, each defined by a specific part (‘sub-trait’) of the

phenotypic trait T. I take it that these parts are dispositions to acquire behavioral

modifications which together amount to a disposition to acquire the new behavior T. The

process he labels ‘genetic assimilation’ is therefore simply the spread of certain of these

phenotypic traits as a result of selection. His trait KG is selectively superior to KL because

6

should be deployed (Moss 2002; Falk 2000; Stotz, Griffiths, and Knight 2004; Griffiths

and Neumann-Held 1999). I will argue here that paying attention to gene concepts helps

one to distinguish two radically different approaches to explaining how the development

of a phenotypic trait can become independent of certain aspects of the developmental

environment. One approach looks to selection to forge a link between the successive

evolution of two developmental pathways to the same trait. The other approach,

represented by Waddington’s genetic assimilation, looks to developmental biology. This

latter approach seeks to explain how the development of a phenotypic trait can become

independent of an environmental stimulus (or become dependent on that stimulus) by

showing that in certain kinds of developmental systems such transitions can be produced

by small genetic changes – changes that are likely to occur spontaneously in a relatively

short time. In the first approach the explanatory focus is on the relative selective

advantage of the two developmental pathways. In the second approach the explanatory

focus is on the developmental mechanisms that make suitable variants available for

selection.

5

Suppose also that at first the KGs are rare. Still, those lucky organisms that have

some TKs genetically fixed by KGs will find it easier to learn the rest of T, and so

will be favoured by natural selection (assuming that learning is here costly).

Selection will thus cumulatively build up the genes KG which genetically fix T.”

(Papineau 2003)

This process has little connection with the one described by Waddington himself2. In

itself this is neither particularly important nor particularly surprising. Many different

processes have been proposed that might free traits from their developmental dependence

on some aspect of the environment, and terms like ‘Baldwin effect’ and ‘genetic

assimilation’ have been used in numerous senses in this extensive literature (See e.g.

Belew and Mitchell 1996; Weber and Depew 2003). In fact, despite calling the process

‘Waddington’s genetic assimilation’ Papineau does not cite Waddington’s work as a

source, but instead cites a well-known computer simulation of the interaction between

learning and inheritance (Hinton and Nowlan 1996). The interesting point is that

Waddington’s actual model of genetic assimilation is simply not accessible to anyone

who conceptualises genes in the way Papineau does in the passage quoted above. Several

recent authors have stressed the need for biologists and philosophers of biology to

become more self-conscious about the existence of multiple gene concepts and of the

appropriate range of theoretical and experimental contexts in which those concepts

2 It does resemble one version of ‘organic selection’. Patrick Bateson has argued that many learningprocesses have components which might separately become independent of the environmental conditionsoriginally required for their development and that the efficiency and/or reliability of the learning processmight thereby be improved. Like Papineau, he points out that these variations would only be selected iforganisms regularly undergo the complete learning process (Bateson 2004, 289).

4

Papineau suggests that this sort of double-strength Baldwin effect will exert powerful

selection pressures in species that exhibit a high degree of social learning. This is an

interesting empirical conjecture that may or may not prove correct. For my part, I am

happy to agree that social learning can play a role in a distinctive form of ‘niche-

construction’ (Odling-Smee, Laland, and Feldman 2003) that can alter selective pressures

in the way Papineau suggests.

I shall say nothing more here about social learning. Rather I want to focus on Papineau’s

discussion of ‘genetic assimilation’. This term was introduced by Conrad H.

Waddington to refer to a specific process (Waddington 1942, 1953). Waddington’s

process stands out among the other ideas listed above (‘organic selection’, ‘coincident

selection’, ‘autonomisation’, ‘the Baldwin effect’) both because its author was able to

demonstrate it in laboratory selection experiments and because it was part of his larger

vision of the relationship between development and evolution, a vision that has

influenced contemporary work in evolutionary developmental biology or ‘evo-devo’.

Let us look more closely at the way Papineau defines “Waddington’s Genetic

Assimilation”. He says:

“Suppose 5 sub-traits, say, are individually necessary and jointly sufficient for T.

Each can either be genetically fixed or acquired through (not necessarily social)

learning. (So for sub-trait TK we have allele KG which genetically fixes TK and

allele KL which allows it to be learned.)

3

focus is on some complex adaptive behaviour, potentially under the control of a suite of

genes at different loci. The challenge is to explain how this suite can get selected in

virtue of their collectively producing the complex adaptive behavior. Prima facie, it

seems that the whole suite of genetic changes would need to occur simultaneously. An

answer becomes available if the complex behaviour is also learnable, for then each gene

can be advantageous on its own, in virtue of making the rest of the behaviour more

quickly or more reliably learnable. The cumulative selection of the whole suite of genes

thus qualifies as a Baldwin effect because it depends essentially on intermediate stages in

which (most of) the behaviour is learned.

This is one part of what Papineau thinks occurs in social learning cases. But he observes

that there is a yet further sense in which such cases fit the Baldwin requirements. The

process he calls ‘genetic assimilation’ takes it as given that the complex behaviour at

issue is indeed learnable. But in many cases it will be puzzling in itself that some

complex behaviour can be learned, at least insofar as instrumental learning is supposed

do the work, and reward only accrues once the whole behaviour is in place. This is

where social learning plays its role: if the behaviour is present in the ‘animal culture’,

then this in itself can render it learnable and so ‘genetically assimilable’. This now gives

us a second sense in which Papineau’s social learning cases are Baldwin effects: the

behaviour is only individually-learnable-and-so-genetically-assimilable because it is

already present as a learned behaviour in the animal culture.

2

typical songs in order to reproduce those songs whilst others do not. Hence we can

envisage a species beginning with one type of developmental pathway and evolving the

other type. If, however, the successive evolution of these two developmental pathways is

a mere coincidence, selection first favoring the ability to acquire the trait and later, quite

independently, favoring the ability to develop it autonomously, then we are not dealing

with a distinctive kind of evolutionary process, but merely with two standard instances of

natural selection. George Gaylord Simpson pointed this out in the paper that gave us the

term ‘Baldwin effect’ (Simpson 1953). The real interest of the Baldwin effect and its

relatives lies in the mechanisms that have been proposed to link the evolution of the two

developmental pathways, so that acquiring the trait through interaction with the

environment makes it more likely that later generations will evolve the ability to acquire

the same trait without that interaction.

Papineau’s paper focuses on the way in which social learning can facilitate such

Baldwin-like links. His basic idea is that genes which accelerate the social learning of

some complex behaviour can become advantageous once that behaviour is present in the

‘animal culture’, even if they were of no advantage when that culture was absent and the

behaviour therefore unlearnable. Here the relevant genes will be selected once the

population is socially transmitting the behaviour, but not otherwise, thus yielding a

scenario that satisfies the specifications of the Baldwin effect. Papineau then subjects

this sort of process to closer analysis, showing that it simultaneously exemplifies two

different kinds of mechanism that the literature recognizes as possible sources of Baldwin

effects. First, there is the process that Papineau calls ‘genetic assimilation’. Here the

1

The Baldwin Effect and Genetic Assimilation: Contrasting

explanatory foci and gene concepts in two approaches to an

evolutionary process1

Paul E. Griffiths,

ARC Federation Fellow and Professor of Philosophy,

School of History, Philosophy, Religion and Classics,

University of Queensland,

Brisbane, QLD 4072,

Australia

1. The Papineau Effect

David Papineau (2003; 2005) discusses the relationship between social learning and the

family of postulated evolutionary processes that includes ‘organic selection’, ‘coincident

selection’, ‘autonomisation’, ‘the Baldwin effect’ and ‘genetic assimilation’. In all these

processes a trait which initially develops in the members of a population as a result of

some interaction with the environment comes to develop without that interaction in their

descendants. It is uncontroversial that the development of an identical phenotypic trait

might depend on an interaction with the environment in one population and not in

another. For example, some species of passerine songbirds require exposure to species-

1 To appear in Proceedings of the Second AHRB Conference on Innateness and the Structure of the Mind,edited by Peter Carruthers, together with a reply by David Papineau.